Our studies have demonstrated that alcohol abuse leads to a decrease in the level of long chain polyunsaturated fatty acids like arachidonate (20:4n6) and docosahexaenoate (22:6n3). For example, there is a selective decrease in the level of 22:6n3 in the livers of rhesus monkeys given alcohol on an ad libitum basis that was associated with the development of liver fibrosis after three years. There is also a loss of docosahexaenoate (DHA) in the brains of cats and rhesus monkeys after chronic alcohol exposure. It is hypothesized that the lowered level of these important cell membrane constituents leads to alterations in cellular function that may underlie some aspects of alcohol-induced organ injuries and that prevention or restoration of this decrement in essential fatty acids may be of therapeutic benefit to alcoholics. Progress has been made in understanding the underlying actions of alcohol on essential fatty acid metabolism. In studies of cats and rhesus monkeys exposed to chronic alcohol, there was a large in increase in markers of lipid peroxidation. However, an increase in the enrichment of long chain polyunsaturates, especially DHA, with deuterium supplied by the 18-carbon fatty acid precursors indicated that essential fatty acid formation and accretion in vivo was increased. This contention is opposite to the commonly held notion that alcohol inhibits desaturase enzymes. These contentions were confirmed in a human study in which it was demonstrated that alcoholics accumulate greater amounts of deuterium- labeled DHA from d5-linolenic acid. These studies support the view that preformed 22:6n3 is essential for proper brain and liver function and that an important mechanism by which alcohol exerts adverse effects is through the antagonism of this fatty acid.